Abstract
Abstract
We have shown that arachidonic acid significantly reduces the production of cleft palate in rats by dexamethasone and that this corrective effect of arachidonic acid is blocked by indomethacin, an inhibitor of cyclooxygenase. Moreover, by using [3H]-arachidonic acid as a tracer we have shown that dexamethasone treatment depresses significantly the free [3H]arachidonic acid available to the microsomal cyclooxygenase in the fetal upper and lower jaws including the palate at the critical period of development. These observations suggest that glucocorticoids produce their palatal teratogenicity by limiting the release and consequently the availability of arachidonic acid at the critical period of development.
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